PP1 peptide
PP1 peptide is an antagonist that specifically binds to scavenger receptor AI (SR-AI), with an IC50 of 29 μM against bovine SR-AI. By recognizing SR-AI which is highly expressed on macrophages, PP1 peptide enables precise targeting and internalization of inflammatory regions within atherosclerotic plaques. PP1 peptide can be used in research related to atherosclerosis.
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- CAS No.: 870274-84-3
- Formule: C79H122N22O22S
- Masse moléculaire:1764.01
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
PP1 peptide (0-300 μM) potently inhibits the binding of SR-AI-targeting phages to immobilized recombinant SR-AI, with an IC50 of 29 μM, and its N-terminal region is critical for activity[1].
The PP1 peptide binds to mouse RAW264.7 macrophages in an SR-AI-dependent manner, as demonstrated by fucoidan-mediated inhibition assays, with an IC50 of 4.2 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
PP1 (0.38 μM; intravenous injection; single administration) selectively targets advanced atherosclerotic plaques in ApoE-/- mice, increases the maximum carrier accumulation by 93.7%, colocalizes with 52.4% of macrophages in plaques, and does not alter plaque size[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ApoE-/- (male, ~65 weeks old, back-crossed for 9 generations on a C57Bl/6 background)[1]
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Dosage:0.38 μM
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Administration:i.v.; single dose
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Result:Showed an 84.12% increase in aortic plaque accumulation compared with untargeted 125I-streptavidin, with no difference in plaque size between groups.
Showed a 93.65% increase in aortic plaque accumulation compared with untargeted Quantumdot Nanocrystals.
Colocalized with 52.4% of intraplaque F4/80-positive macrophages, compared with 6.3% for untargeted Quantumdots.
Chemical Information
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CAS No. 870274-84-3
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Masse moléculaire 1764.01
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Formule C79H122N22O22S
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SMILES
O=C(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC1=CC=CC=C1)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CS)C(N[C@@H](CC2=CNC3=CC=CC=C23)C(N[C@@H](CO)C(N[C@@H](CC(O)=O)C(N[C@@H](C)C(N4[C@@H](CCC4)C(N[C@@H](C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CC(C)C)N
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Sequence
Leu-Ser-Leu-Glu-Arg-Phe-Leu-Arg-Cys-Trp-Ser-Asp-Ala-Pro-Ala
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Sequence Shortening
LSLERFLRCWSDAPA
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)